BACKGROUND: The phenomenon of silent hypoxaemia has been described in patients with COVID-19 pneumonia, which is characterised by low oxygen saturation levels of <90% in those who appear clinically well and do not show signs of significant respiratory distress.OBJECTIVES: To assess the impact on clinical outcomes for high-risk COVID-19 patients using a pulse oximeter to monitor oxygen saturation levels in a home setting.METHODS: We performed a retrospective cohort analysis using data from a large South African insurance administrator. Patients were categorised as high risk, based on age and specific underlying clinical conditions, or from predictive models derived from medical scheme administrative claims data. The impact of pulse oximetry home monitoring on COVID-19 clinical outcomes was investigated by the use of Cox proportional hazard models.RESULTS: Between 2 March 2020 and 31 October 2020, of 38 660 patients analysed, 8 115 were in the intervention group. The 60-day mortality rate for the evaluated high-risk population was 1.35%. After adjusting for age and comorbidity differences, the intervention group was found to have an adjusted hazard ratio of 0.52 (p<0.0001). No statistical significance was found between the intervened and control groups for admission to hospital, admission to intensive care unit (ICU) and use of mechanical ventilation. The intervention group had a lower median C-reactive protein (CRP) level on admission (p=0.03). After adjustment for admission CRP levels, elevated CRP was associated with an increased mortality (p<0.0001), while the statistical significance in mortality between the intervention and the control group was lost.CONCLUSIONS: High-risk COVID-19 patients who used a pulse oximeter to monitor oxygen saturation levels had significantly lower mortality rates compared with other high-risk patients. The mortality benefit may be explained by earlier presentation to hospital, as suggested by lower initial CRP levels.

OBJETIVO: Quantificar a concentração de glicosaminoglicanas sulfatadas (GAGs) no líquido sinovial (LS) de joelhos com ruptura crônica do ligamento cruzado anterior (LCA) e identificar uma possível correlação entre a concentração de GAGs no LS e o tempo pós-ruptura e grau de lesão condral. MÉTODOS: Foram avaliados 14 indivíduos adultos do sexo masculino com ruptura total unilateral do LCA, ocorrida entre cinco a 144 meses. Todos os sujeitos foram puncionados, sendo possível a coleta de LS em dez indivíduos. As amostras foram quantificadas para determinar a concentração de GAGs usando a coloração azul de dimetilmetileno, método descrito por Farndale21. O grau de lesão condral foi macroscopicamente avaliado pela escala histológica de Mankin modificada por Messner14. As correlações entre concentração de GAGs e lesão condral foram feitas pelo teste de correlação de Sperman (p< 0,05) e a concentração de GAGs e tempo pós-ruptura pelo teste de correlação de Pearson (p< 0,05). RESULTADOS: Concentração de GAGs no LS apresentou variação média de 73,84 ± 40,75µg/mL, sendo o tempo médio pós-ruptura de 40,4 + 40,3 meses. Não houve correlação entre concentração de GAGs e o tempo pós-ruptura (r= -0,09, p= 0,81). Os graus de lesão condral encontrados foram de 0, 1, 4 e 5. Não houve correlação entre grau de lesão condral e a concentração de GAGs no LS (r= -0,41, p= 0,24). CONCLUSÕES: Após no mínimo cinco meses, a concentração de GAGs no LS de joelhos com ruptura do LCA independe do tempo pós-ruptura e/ou do grau de lesão condral.

OBJECTIVE: To quantify the concentration of sulfated glycosaminoglycans (GAGs) concentration in the synovial fluid (SF) of knees with chronic anterior cruciate ligament (ACL) rupture and to identify possible associations between GAG concentration in SF and the time elapsed since rupture and degree of chondral injury. METHOD: Fourteen adult male subjects with total unilateral ACL rupture, which had occurred between 5 and 144 months earlier, were assessed. All subjects underwent joint aspiration; it was possible to collect SF from ten individuals. The samples were quantified to determine the GAG concentration using dimethylmethylene blue (DMMB) staining. The degree of chondral injury was macroscopically evaluated using the modified Mankin histological scale. Spearman correlation test (< 0.05) was used to evaluate the association between GAG concentration and chondral injury, and Pearson correlation test (< 0.05) was used to evaluate the association between GAG concentration and the time elapsed since rupture. RESULTS: The GAG concentration in SF showed a mean variation of 73.84 ± 40.75 µg/ml, with a mean time of 40.4 ± 40.3 months since the rupture. There was no correlation between GAG concentration and time since the rupture (r= -0.09, p= 0.81). The chondral injury grades found were 0, 1, 4 and 5. There was no correlation between chondral injury grade and GAG concentration in SF (r= -0.41, p= 0.24). CONCLUSION: After at least 5 months, the GAG concentration in SF from knees with ACL rupture is independent of the time elapsed since rupture and/or the severity of chondral injury.

La enfermedad cerebrovascular (ECV) es la tercera causa de muerte en países industrializados. De todos los tipos de EVC, la hemorragia subaracnoidea (HSA) es responsable de 22% a 29% de la mortalidad. Alrededor de 30% de los pacientes con hemorragia subaracnoidea (HSA) secundaria a ruptura de aneurisma cerebral, desarrollan vasoespasmo arterial y con ello el déficit neurológico asociado aumenta. Esta complicación empeora el pronóstico de los pacientes, puesto que un 25% de ellos mueren y otro 30% a 35% sufren de déficit neurológico permanente. Entonces, el vasoespasmo cerebral es el factor modificable más importante para mejorar la tasa de morbimortalidad en pacientes con hemorragia subaracnoidea secundaria a ruptura de aneurisma. Estos puntos nos obligan a definir esquemas de intervención bien desarrollados y esquematizados, en donde el primer objetivo sea la prevención, permitiendo hacer un diagnóstico ultra temprano y que incluya un esquema de intervención bien definido que pueda ayudar a frenar el curso de la devastadora historia natural de esta complicación.

The cerebrovascular disease (CVD) is the third cause of death in industrializad countries. Of all the types of CVD, the subarachnoid hemorrhage (HAS) is responsible from 22% to 29% of mortality. Around 30% of the patients with secondary subarachnoid hemorrhage (HAS) to rupture of cerebral aneurism develops arterial vasospasm and with it the associated neurological deficit increases. This complication the prediction of the patients, since 25% of them die and another 30 to 35% undergo permanent neurological deficit. Then, cerebral vasospasm is the modified factor more important to improve the rate of morbidity and mortality in patients with secondary HAS dur to aneurism rupture. These points compel us to define schemes of developed intervention directed to prevention allowing to make do an early extreme diagnosis that includes defined schemes of intervention that help to restrain the course of the devastating natural history of this complication.